Therapeutic Effect of Metformin and Vitamin E Versus Prescriptive Diet in Obese Adolescents with Fatty Liver

2011 ◽  
Vol 81 (6) ◽  
pp. 398-406 ◽  
Author(s):  
Akcam ◽  
Boyaci ◽  
Pirgon ◽  
Kaya ◽  
Uysal ◽  
...  

Objective: The aim of the study was to determine whether metformin or vitamin E treatment for six months is effective in reducing body weight, blood pressure, and also ameliorating insulin resistance, adiponectin, and tumor necrosis factor (TNF)-alpha in obese adolescents with non-alcoholic fatty liver disease (NAFLD). Methods: Sixty-seven obese adolescents with liver steatosis (age range, 9 - 17 years) were included in the study. The metformin group received an 850-mg dose of metformin daily and the vitamin E group received 400 U vitamin E /daily, in capsule form for 6 months, plus an individually tailored diet, exercise, and behavioral therapy. Results: After 6 months later, there was a significant decline in body mass index, and fasting insulin and homeostatic model assessment (HOMA) values in all three groups. Moreover, in comparingson of changes in HOMA among the groups, the metformin- treated group showed significantly improved metabolic control and insulin sensitivity (HOMA) at the end of the study. There were no significant differences for changes of adiponectin, TNF-alpha, in all three groups after 6 months study. Conclusion: These data suggest that metformin treatment is more effective than dietary advice and vitamin E treatment in reducing insulin resistance, and also in ameliorating metabolic parameters such as fasting insulin and lipid levels, in obese adolescents having NAFLD.

2021 ◽  
Vol 53 (02) ◽  
pp. 100-104
Author(s):  
Amr Ali El-Sehrawy ◽  
Omnia State ◽  
Rasha Rizk Elzehery ◽  
Ahmed Salem Mohamed

AbstractIt is suggested that estrogen protects premenopausal women against non-alcoholic fatty liver disease. From another perspective, the relation between metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD) is bidirectional. Role of insulin resistance (IR) in NAFLD continues to be a matter of debate. The present study aimed to assess the relation between IR and NAFLD in premenopausal women with MetS. The study included 51 premenopausal women with MetS. In addition, there were 40 age-matched healthy controls. All participants were subjected to careful history taking and thorough clinical examination. Performed laboratory investigations included fasting blood glucose, fasting insulin, lipid profile, and liver functions. Calculation of IR was achieved by the Homeostasis Model Assessment (HOMA-IR). NAFLD was graded into three grades according to findings of abdominal ultrasound. Patients had significantly higher BMI, SBP, DBP, FBG, fasting insulin, HOMA-IR, total cholesterol, triglycerides, and LDL levels when compared with controls. They also had significantly lower HDL levels in comparison to controls. Moreover, they have more advanced grades of NAFLD in contrast to controls. Comparison between patients with various grades of NAFLD regarding the clinical data revealed significant increase of fasting insulin and HOMA-IR levels with advancing NAFLD grade. Using multivariate regression analysis, HOMA-IR was an independent predictor of advanced NAFLD grade. In conclusion, the present study documented a combined inter-relation between MetS, IR, and NAFLD in premenopausal women with MetS. IR is correlated with NAFLD grade.


2019 ◽  
Vol 8 (12) ◽  
pp. 2157 ◽  
Author(s):  
Eline H. van den Berg ◽  
Eke G. Gruppen ◽  
Hans Blokzijl ◽  
Stephan J.L. Bakker ◽  
Robin P.F. Dullaart

A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Dietary sodium intake was measured by sodium excretion in two complete consecutive 24 h urine collections in 6132 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Fatty Liver Index (FLI) ≥60 and Hepatic Steatosis Index (HSI) >36 were used as proxies of suspected NAFLD. 1936 (31.6%) participants had an FLI ≥60, coinciding with the increased prevalence of type 2 diabetes (T2D), metabolic syndrome, hypertension and history of cardiovascular disease. Sodium intake was higher in participants with an FLI ≥60 (163.63 ± 61.81 mmol/24 h vs. 136.76 ± 50.90 mmol/24 h, p < 0.001), with increasing incidence in ascending quartile categories of sodium intake (p < 0.001). Multivariably, an FLI ≥60 was positively associated with a higher sodium intake when taking account for T2D, a positive cardiovascular history, hypertension, alcohol intake, smoking and medication use (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.44–1.64, p < 0.001). Additional adjustment for the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) diminished this association (OR 1.30, 95% CI 1.21–1.41, p < 0.001). HSI >36 showed similar results. Associations remained essentially unaltered after adjustment for body surface area or waist/hip ratio. In conclusion, suspected NAFLD is a feature of higher sodium intake. Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake.


2018 ◽  
Vol 23 (2) ◽  
pp. 84
Author(s):  
Eunice Limantara ◽  
Felicia Kartawidjajaputra ◽  
Antonius Suwanto

Early detection of insulin resistance (IR) or non-alcoholic fatty liver disease (NAFLD) is crucial to preventing future risks of developing chronic diseases. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Liver Fat Score (LFS), and Fatty Liver Index (FLI) are generally employed to measure severity stages of IR and NAFLD. The study of gene expressions could explain the molecular mechanisms that occur early on in IR and NAFLD; thus providing potential early markers for both diseases. This study was conducted to evaluate the gene expressions that could potentially be early markers of IR and NAFLD. All participants (n = 21) had normal blood glucose and were categorized as without hepatosteatosis (n = 10), at higher risk of hepatosteatosis (n = 6), and hepatosteatosis (n = 5). Gene expression analysis was performed using the 2-∆∆CT relative quantification method. There were significant differences in galnt2 (p < 0.002) and sirt1 (p < 0.010) expression between the first and the third tertiles of HOMA-IR; and in ptpn1 (p < 0.012) expression between the first and the second tertiles of LFS. In conclusion, the expressions of galnt2 and sirt1 could be used as early markers of IR, while the expression of ptpn1 could be employed as an early marker of NAFLD.


2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Emine Turkkan ◽  
Huseyin Dag ◽  
Okan Dikker ◽  
Nevin Cetin Dag ◽  
Alper Kacar ◽  
...  

Background: Omentin-1 is an adipocytokine secreted from visceral adipose tissue that is thought to increase insulin sensitivity. Non-alcoholic fatty liver disease (NAFLD) is a comparatively extensive problem in obese adolescents. Decreased omentin-1 levels have been reported in obese patients, but the relationship between NAFLD and omentin-1 is contradictory. Objectives: We aimed to evaluate the omentin-1 levels in the sera of obese adolescents with and without NAFLD and compare them with each other. Methods: In this study, a total of 88 adolescents (56 obese and 32 normal-weight) were enrolled. Abdominal ultrasonography (US) identified 28 obese adolescents with grade 2-3 hepatosteatosis constituting the NAFLD group and 28 without hepatosteatosis on US constituting the non-NAFLD group. The control group included 32 age- and gender-matched cases without hepatosteatosis and with normal percentile body mass index (BMI). Serum omentin-1 levels were evaluated and compared. Results: The mean age of the research group was 12.72 ± 1.91 years. Unsurprisingly, BMI, glycated hemoglobin (HbA1c), liver transaminases (AST, ALT), total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL), homeostatic model assessment for insulin resistance (HOMA-IR), and insulin rates were noticeably elevated in obese adolescents compared to controls (P < 0.05). However, omentin-1 and high-density lipoprotein cholesterol (HDL) levels were remarkably lower in the obese group (P < 0.05). No significant difference was found between the NAFLD and non-NAFLD groups regarding omentin-1, HbA1c, glucose, urea, creatinine, AST, C-reactive protein (CRP), total cholesterol, triglyceride, HDL, LDL, thyroid stimulating hormone, 25-hydroxyvitamin D3, HOMA-IR, and insulin. The BMI and ALT grades of the non-NAFLD group were notably lower than the NAFLD group (P < 0.05). While there was no significant difference between omentin-1 and other parameters in obese adolescents without NAFLD (P > 0.05), we found a significant difference between omentin-1 and BMI, AST, ALT, HOMA-IR, and insulin values in obese adolescents with NAFLD (P < 0.05). Conclusions: Omentin-1 levels were decreased in obese adolescents regardless of the presence of NAFLD. However, in obese patients with NAFLD, there was a significant difference between omentin-1 and several markers of obesity and insulin resistance.


2021 ◽  
Vol 11 (1) ◽  
pp. 41
Author(s):  
Hwi Seung Kim ◽  
Yun Kyung Cho ◽  
Eun Hee Kim ◽  
Min Jung Lee ◽  
Chang Hee Jung ◽  
...  

The triglyceride glucose (TyG) index has been suggested as a marker for insulin resistance; however, few studies have investigated the clinical implications of markers that combine obesity markers with the TyG index. This study aimed to investigate the associations between non-alcoholic fatty liver disease (NAFLD) and TyG-related markers in healthy subjects in Korea. We enrolled 21,001 asymptomatic participants who underwent hepatic ultrasonography. The homeostasis model assessment of insulin resistance (HOMA-IR), TyG index, TyG-body mass index, and TyG-waist circumference (WC) were subsequently analyzed. NAFLD was diagnosed using hepatic ultrasonography. A multiple logistic regression analysis was performed to evaluate the associations between the quartiles of each parameter and the risk of NAFLD. The increase in the NAFLD risk was most evident when the TyG-WC quartiles were applied; the multivariate-adjusted odds ratios for NAFLD were 4.72 (3.65–6.10), 13.28 (10.23–17.24), and 41.57 (31.66–54.59) in the 2nd, 3rd, and 4th TyG-WC quartiles, respectively, when compared with the lowest quartile. The predictability of the TyG-WC for NAFLD was better than that of the HOMA-IR using the area under the curve. The TyG-WC index was superior to the HOMA-IR for identifying NAFLD in healthy Korean adults, especially in the non-obese population.


2020 ◽  
Vol 20 (10) ◽  
Author(s):  
Hossein Moameri ◽  
Zahra Akbarzade ◽  
Elmira Khamisi ◽  
Saeed Osati ◽  
Alireza Ghaemi ◽  
...  

Background: Insulin resistance can be a predictor of adverse fatty liver disease and health problems. Objectives: The present study aimed to investigate the effect of insulin resistance on fatty liver disease. Methods: This study used the data of 2,160 individuals registered in a cross-sectional study who were randomly selected from among clients of a nutrition clinic in Tehran from April to December 2019. Insulin resistance and beta-cell activity were calculated by the homeostasis model assessment formula. The study outcome was defined as having fatty liver disease. The odds ratio (95% CI) was calculated using logistic regression models. Results: The mean age was 35 (± 9) in healthy subjects and 49 (± 8) in fatty liver disease patients (age range: 16 to 42 years). Nearly 34.5% of the individuals had fatty liver disease. According to the adjusted results of the logistic regression model, the risk of NAFLD was 1.05 (P < 0.001) for one unit increase in fasting insulin and 1.01 (P < 0.001) for one unit increase in 2-h insulin, which indicated the statistically significant relationship of NAFLD with fasting insulin and 2-h insulin. Also, the risk of NAFLD was 1.01 P < 0.001) for one unit increase in FPG, which was statistically significant. Moreover, the adjusted risk of NAFLD was 1.00 (P < 0.001) for one unit increase in 2-h glucose, which was not statistically significant. Finally, the adjusted risk of NAFLD was 1.29 (P < 0.001) for one unit increase in HOMA-IR, which was statistically significant. Conclusions: The findings of the present study demonstrated that insulin resistance could increase the risk of fatty liver disease. Also, each one-unit increase in fasting blood sugar, fasting insulin, and 2-h insulin increased the risk of fatty liver disease. Therefore, the results of this study may be useful for health policymakers to design suitable preventive and therapeutic interventions for those with NAFLD to prevent and control this disease.


2014 ◽  
Vol 3 (1) ◽  
Author(s):  
Yusri Diane Jurnalis ◽  
Yorva Sayoeti ◽  
Elfitrimelly Elfitrimelly

AbstrakNonalcoholic Fatty Liver Disease (NAFLD) merupakan penyebab tersering penyakit hati kronik pada anak dan remaja diseluruh dunia. NAFLD berhubungan dengan obesitas, diabetes melitus tipe 2 dan sindrom metabolik. Resistensi insulin memegang peranan penting dalam patogenesis molecular terjadinya NAFLD. Ketidakseimbangan prooksidan dan antioksidan pada sel hepatosis menentukan progresifitas penyakit ini. Sebagai antioksidan telah dilakukan penelitian mengenai efek antioksidan vitamin E, vitamin C, betaine, N-asetil sistein, probucol dan silymarin. Antioksidan tersebut memperlihatkan perbaikan fungsi hepar dan gambaran histopatologis.Kata kunci: Arial 9 NAFLD, resistensi insulin, antioksidanAbstractNonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in pediatric and adolescent population. NAFLD related with obesity, type 2 diabetes mellitus and metabolic syndrome. Insulin resistance and oxidative stress have important role in molecular pathogenesis of NAFLD. Prooxidant and antioxidant factor in hepatosit can determine progressivity of liver disease. As antioxidant agent for treatment NAFLD have been studied effect of vitamin E, vitamin C, betaine, N-acetyl cystein, probucol and sylimarin. They have been shown improvement of liver function test and histopathologycal feature.Keywords:NAFLD, insulin resistance, antioxidant


Sign in / Sign up

Export Citation Format

Share Document